HM Kim

Thin and flexible composite films of raw or purified multiwalled carbon nanotube (MWCNT) with various mass fractions and poly(methylmethacrylate) (PMMA) were synthesized for electromagnetic interference (EMI) shielding material. From scanning electron microscopy and high-resolution transmission electron microscopy photographs, we observed the formation of a conducting network through MWCNTs in an insulating PMMA matrix and the existence of an Fe catalyst in MWCNTs. The dc conductivity (σdc) of the systems increased with increasing MWCNT mass fraction, showing typical percolation behavior. The measured EMI shielding efficiency (SE) of MWCNT–PMMA composites by using the extended ASTM D4935-99 method (50 MHz–13.5 GHz) increased with increasing MWCNT mass fraction as σdc. The highest EMI SE for raw MWCNT–PMMA composites was ∼27 dB, indicating commercial use for far-field EMI shielding. The contribution of absorption to total EMI SE of the systems is larger than that of reflection. Based on magnetic permeability, we suggest raw MWCNTs and their composites can be used for near-field EMI shielding.

Homozygous mutant rats at the newly found white spotting (Ws) locus were anemic and deficient in mast cells and melanocytes. Because the phenotype of Ws/Ws rats resembled the phenotype of mice possessing a double-gene dose of mutant alleles at the W locus and because the c-kit gene was mapped at the W locus of mice, we characterized the c-kit gene of Ws/Ws rats. The authentic sequence of the rat c-kit cDNA was determined by using a cDNA library prepared from the hippocampus of Sprague-Dawley rats. The c-kit cDNA of Ws/Ws and normal (+/+) control rats was obtained by reverse transcriptase modification of the polymerase chain reaction. When compared with the authentic sequence, a deletion of 12 bases was found in the c-kit cDNA of Ws/Ws rats. This change was shown to be a result of the deletion of the genomic DNA. Four amino acids encoded by the deleted 12 bases (ie, Val-Lys-Gly-Asn) were located at two amino acids downstream from the tyrosine autophosphorylation site in the c-kit kinase and were conserved not only in mouse and human c-kit kinases but also in mouse and human c-fms kinases (ie, receptors of colony-stimulating factor-1). Taken together, the Ws/Ws rat is the first characterized mutant of the c-kit gene in an animal species other than the mouse.

TGF-beta1 is a member of a family of polypeptide factors that control proliferation, differentiation, chemotaxis, and other functions in many cell types. TGF-beta1 has been shown to inhibit many immunologic functions. However, here we report that TGF-beta1 has an important role in the elicitation of IgE-dependent allergic reactions. The synthetic antisense TGF-beta1 oligonucleotides dose-dependently inhibit passive cutaneous anaphylaxis (PCA) reaction and histamine release from the mast cells activated by anti-DNP IgE in rats. The level of cAMP in mast cells, when antisense TGF-beta1 oligonucleotides was added, significantly increased approximately 7-fold compared with that of basal cells. The antisense TGF-beta1 oligonucleotides also had a significant inhibitory effect on anti-DNP IgE-induced TNF-alpha release from mast cells. In situ hybridization analysis showed that the PCA reaction sites treated with antisense TGF-beta1 oligonucleotides exhibited no detectable levels of TGF-beta1 and L-histidine decarboxylase mRNA after anti-DNP IgE stimulation, whereas the PCA reaction sites treated with sense TGF-beta1 oligonucleotides possessed significant amounts of their mRNA. Additionally, neutralizing Ab to TGF-beta1 blocked the PCA reaction significantly, but its Ab did not inhibit peritoneal mast cell-released histamine upon treatment with anti-DNP IgE. Our results suggest that TGF-beta1 is critical to the development of IgE-dependent anaphylaxis reactions.

OBJECTIVES: β-Phenylethyl isothiocyanate (PEITC) has been demonstrated to fight many types of cancers through various molecular pathways. In this study, we focused on its effect on the induction of apoptosis to inhibit cell growth and molecular mechanism in oral cancer. MATERIALS AND METHODS: 3-(4,5-dimethylthiazol-2-yl)-5-(2,4-disulfophenyl)-2-(4 sulfophenyl)-2H-tetrazolium (MTS) assay was used to examine cell viability. The apoptotic effect was investigated using 4'-6-Diamidino-2-phenylindole (DAPI) staining or Western blotting. Inhibitors were used to determine the molecular target and mechanism of PEITC-mediated apoptosis. RESULTS: β-Phenylethyl isothiocyanate inhibited the growth of HN22 human oral cancer cells and induced caspase-dependent apoptosis in HN22 cells as evidenced by nuclear fragmentation and the activation of caspase 3. It increased cleaved caspase 8, truncated BID, and death receptor 5 (DR5) through the activation of p38 MAPK. This result was confirmed by blockage of PEITC-induced cleavages of Poly(ADP-ribose) Polymerase, caspase-3, caspase-8, and DR5 by p38 MAPK inhibitor, SB203580. We also found that PEITC activated p38 and augmented DR5 to induce apoptosis in other human oral cancer cells. CONCLUSIONS: These results suggest that DR5 is a potential molecular target for PEITC-induced apoptosis in oral cancer via p38 MAPK.

Ws/Ws rats have a small deletion at the tyrosine kinase domain of the c-kit gene, and practically no mast cells were detectable when the tissues were stained with alcian blue. Because alcian blue stains proteoglycans, there is a possibility that immature mast cells that do not contain a sufficient amount of proteoglycans are not detectable by this method. We examined this possibility by using other markers of mast cells. The histamine content in the skin of Ws/Ws rats was 0.3% that of control normal (+/+) rats. Because the number of alcian blue-positive mast cells in the skin of Ws/Ws rats was also 0.3% that of +/+ rats, histamine in the skin seemed to be concentrated to alcian blue-positive mast cells. Mast cells in the skin of +/+ rats express messenger RNA of Fc epsilon RI beta-subunit and c-kit protein. Because c-kit messenger RNA was normally expressed at least in the brain of Ws/Ws rats despite the small deletion, we examined the expression of Fc epsilon RI beta-subunit and c-kit messenger RNA in the skin and stomach of Ws/Ws rats by reverse transcriptase modification of polymerase chain reaction. Expression of either Fc epsilon RI beta-subunit or c-kit messenger RNA in the skin and stomach of Ws/Ws rats was estimated to be less than 1% that of +/+ rats. Moreover no Fc epsilon RI beta-subunit-expressing and no c-kit-expressing cells were detectable in the skin of Ws/Ws rats by in situ hybridization histochemistry. The present result suggests the absence of immature mast cells in tissues of Ws/Ws rats.